The Third Heart Sound October 1999 - The presence of S3 may be the earliest clue to left ventricular failure. It predicts a high risk of complications in noncardiac surgery and is a predictor of response to digoxin in CHF patients. However, the variation in its detection is high even among experienced doctors. While the presence of S3 may have important clinical implications, high variation in detecting might limit its use. Long version Although diagnostic testing has vastly improved, many diagnoses can be made by a history and physical exam. As attention gets more focused on cost-effective health care, the art of physical examination has greater significance. The third heart sound (S3) is a physical sign with important implications. In this review, I tried to compile current information on S3, especially its clinical use. I searched Medline from 1966 to the present for articles under "heart sounds" "heart failure" and "heart auscultation". Several textbook and journal articles published before 1966 were also reviewed in detail. Data were extracted in these categories: 1) general information and history 2) pathophysiology and mechanism of production 3) clinical examination 4) clinical importance 5) reliability of clinical assessment. In 1856, Potain first described "gallop rhythm" as an audible phenomenon in which a tripling or quadrupling of heart sounds resembles the canter of a horse. That term is still used to describe a third or fourth heart sound. Gallops are diastolic events and seem to be related to 2 periods of filling of the ventricles: 1) the rapid filling phase (ventricular diastolic gallop or S3) 2) the presystolic filling phase related to atrial systole (atrial gallop or S4) Gallop rhythm, especially S3, is well recognized as an early clue to the presence of heart disease and may offer valuable information about diagnosis, prognosis, and treatment. S3 occurs 0.12 to 0.16 seconds after the second heart sound. Potain suggested that it results from the sudden stop of distention of the ventricle at the end of the rapid filling phase of diastole: "If the cardiac muscle has lost its tone, the ventricle, in dilating, quickly arrives at a point where the fibrous resistance of its wall limits its distention and then, abruptly stopped, produces a tension - a shock and the gallop sound." It is agreed that S3 is associated with over-distention of the ventricle during the rapid early filling phase. Early work in the 1960s focused on early ventricular filling being the most likely cause. In contrast, a mitral valve origin (partial, momentary closure of the mitral valve during early diastole) was suggested by Dock and later supported by several authors. This theory fell from favor with reports that the mitral valve structure was not necessary for S3 to occur. Gionelly reported its presence in several patients with biologic replacement valves. Coulshed and Epstein returned to the original Potain theory: "Our evidence supports the original concept of Potain that S3 is produced when the rapidly distending ventricle reaches a point when its distention is checked by the resistance of its wall and the ensuing vibrations are audible as the third heart sound." By the early 1980s, there was renewed interest in the theory of a built-in limit to the longitudinal expansion of the left ventricular wall as causing S3. Studying pulsed Doppler measurement of left ventricular filling in people with third heart sounds, Pozzoli confirmed that the rapid deceleration of left ventricular inflow at the end of early diastole is the most likely cause of S3. Van de Werf, studying left ventricular blood flow in early diastole using cardiac cath in humans, showed that all patients with S3 had increased rapid filling waves that were nearly identical. They suggested that the steep left ventricular pressure increase in early diastole causes a reversal of the transmitral pressure gradient and hence a more rapid deceleration of inflow. Since the vibrations of S3 occur during deceleration of inflow, a conversion of kinetic into vibratory energy is likely. These vibrations are audible if transmitted with enough intensity. The higher the inflow rate (valve regurgitation - high output states) and the steeper the rapid filling wave (high filling rates), the greater the deceleration and more likely an S3 will occur. S3 in young adults may be explained by the relatively large motion of the heart and the thin chest wall in such subjects. Any theory should explain the disappearance of S3 with aging. Van de Werf suggested an age- related increase in blood pressure and relative left ventricular hypertrophy (and resulting decrease in early diastolic filling) to account for this. Kupari disagreed, attributing this to an age related reduction of left ventricular early diastolic function. Most gallop sounds are faint. The patient should be lying down and examined in a quiet room. Left sided S3 is best heard at the apex of the heart, with the patient in the left lateral position. It is a low-pitched sound and heard best using the bell of the stethoscope applying light pressure. It follows the second heart sound in timing. S4 occurs before and S3 after the carotid up-stroke. It is more easily heard after mild exertion, in the presence of a fast heart rate from any cause and also with elevation of the legs. The factors that usually prevent S3 detection are surrounding noise, obesity, emphysema, failure to apply the bell precisely to the cardiac apex, too much pressure with the bell (which dampens low frequency sound), and examining the patient in a seated position. Simple maneuvers like closing the door to the exam room to reduce ambient noise will help in detecting S3. If the heart rate is higher than 100 beats per minute, finding third and fourth heart sounds is impossible. Unless the heart rate is slowed, the examiner can only guess at telling S3 from S4, unless there is a-fib, which precludes an S4. S3 is heard in several illnesses. It can normally be heard in children and adults up to age 40. Authors have reported its presence in 20-93% of healthy volunteers. Although teaching has been that an S3 heard after 40 years of age indicates illness, several factors may influence audibility. S3 is more often heard in adults who are very lean. S3 is heard normally in 80% of pregnant women. The most useful and best accepted clinical importance of S3 is in detecting left-sided heart failure, especially in the early stages when other signs may be normal. In 1968, Shah studied patients with heart disease and noted that the presence of S3 detected patients with elevated end-diastolic pressures and decreased cardiac output. In a later study of patients with aortic valve disease, the same authors again noted S3 associated with left ventricular failure. Harvey and Stapleton first noted that the presence of an S3, even without other signs of cardiac decompensation, identified patients who are prone to pulmonary edema after a surgical procedure. More recently, S3 was the best predictor of response to digoxin in CHF patients. Patel compared stethescope findings of S3 with MUGA analysis of heart function. The authors concluded that presence of an S3 was highly predictive of abnormal EF. The absence of S3, however, is not uncommon in patients with mildly impaired ejection fraction. Presence of S3 in patients with valve disease is often regarded as a sign of heart failure. However, in patients with mitral regurgitation, S3 does not necessarily mean left ventricular failure. Mitral regurgitation augments early diastolic filling and can therefore lead to S3 without left ventricular failure. It is common to hear an S3 after acute heart attack. This usually disappears several days or weeks afterward. Persistent S3 after this time may signify more severe heart damage. Glover and Littler noted that S3 was one factor influencing mortality in patients with chronic ischemic heart failure. In a study of patients awaiting heart transplant, presence of S3 was one of 7 independent factors predicting a poor prognosis. Held compared the ability of 4 groups of observers - cardiologists, residents, nurses, and students - to detect third heart sounds. He found that the detection rate increased with the experience of the observer. While success was highest for cardiologists, variation of ability to detect S3 was considerable even among experienced cardiologists. Another study on inpatients with heart conditions studied S3 detection by 4 observer groups - a board certified internist, an internist trainee, a cardiologist trainee, and a board certified cardiologist. Each patient was observed by at least one pair of the above. They found that if one observer heard an S3, the probability of detection by a second observer was only 34-38%. Gadsboll also reported poor inter-observer agreement on S3, in assessing heart failure in heart attack patients. Conclusions The third heart sound is a low-pitched sound after the second heart sound and corresponds in timing to rapid ventricular filling in early diastole. It is best heard at the mitral area, with the patient lying in the left lateral position. While it may be heard normally in individuals under 40 years old, its presence beyond this age usually means a heart problem. Its presence may have important diagnostic implications. It may be the earliest clue to the presence of left ventricular failure. It predicts higher risk of complications in noncardiac surgery and is a predictor of response to digoxin in patients with CHF. Its presence in patients with chronic aortic regurgitation reflects left ventricular dysfunction and may be useful for selecting patients for cardiac cath and valve replacement. A persistent S3 after heart attack indicates a poor prognosis. Although observer variation in its detection is high, when detected, it has definite clinical implications. Nirmal Joshi, MD General Internal Medicine, Milton S. Hershey Medical Center Pennsylvania State University South Med J 92(8):756-761, 1999